ArticleHaematologica2022
Deregulation of JAK2 signaling underlies primary cutaneous CD8
Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Cutaneous T-cell lymphomas and dupilumab for atopic dermatitis: A systematic review and expert consensus.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Pooled it
- Transcriptome differences in lesions by color, and cancer mutations in endometriosis.Reproduction & fertility · 2026Article
- Review
- Pediatric Primary Cutaneous CD8+ Aggressive Epidermotropic Cytotoxic T-Cell Lymphoma With Unusually Long Clinical Course.Journal of cutaneous pathology · 2026Article
- Cutaneous and Systemic Complications in Primary CD8+ Aggressive Epidermotropic Cytotoxic T-cell Lymphoma.Cureus · 2025Article
- Primary Cutaneous CD8+ Aggressive Epidermotropic Cytotoxic T-Cell Lymphoma: A Rare and Aggressive Case Report with Clinical and Pathological Insights.Journal of clinical medicine · 2025Article
- Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma with novel FGFR1 fusion treated with pemigatinib.Blood advances · 2025Article
- Single-cell RNA sequencing comparison of CD4+, CD8+ and T-cell receptor γδ+ cutaneous T-cell lymphomas reveals subset-specific molecular phenotypes.The British journal of dermatology · 2025Article
- Advances in Novel Systemic Therapies for the Management of Cutaneous T Cell Lymphoma (CTCL).Current hematologic malignancy reports · 2025Review
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Through thick and thin: confronting the aggressive cutaneous T-cell lymphomas.Hematology. American Society of Hematology. Education Program · 2024Review
- Update on primary cutaneous T-cell lymphomas rare subtypes.Dermatology reports · 2024Review
- JAK Inhibitors in Cutaneous T-Cell Lymphoma: Friend or Foe? A Systematic Review of the Published Literature.Cancers · 2024Review
- Diverse and reprogrammable mechanisms of malignant cell transformation in lymphocytes: pathogenetic insights and translational implications.Frontiers in oncology · 2024Review
- Primary Cutaneous Multifocal Indolent CD8+ T-Cell Lymphoma: A Novel Primary Cutaneous CD8+ T-Cell Lymphoma.Biomedicines · 2023Article
- Recent advances in cutaneous lymphoma-implications for current and future classifications.Virchows Archiv : an international journal of pathology · 2023Review
- Review
- Advances in the understanding and treatment of Cutaneous T-cell Lymphoma.Frontiers in oncology · 2022Review
- Safety and Danger Considerations of Novel Treatments for Atopic Dermatitis in Context of Primary Cutaneous Lymphomas.International journal of molecular sciences · 2021Review
- Primary cytotoxic T-cell lymphomas harbor recurrent targetable alterations in the JAK-STAT pathway.Blood · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma (pcAECyTCL) is a rare variant of cutaneous T-cell lymphoma with an aggressive clinical course and a very poor prognosis. Until now, neither a systematic characterization of genetic alterations driving pcAECyTCL has been performed, nor effective therapeutic regimes for patients have been defined. Here, we present the first highresolution genetic characterization of pcAECyTCL by using wholegenome and RNA sequencing. Our study provides a comprehensive description of genetic alterations (i.e., genomic rearrangements, copy number alterations and small-scale mutations) with pathogenic relevance in this lymphoma, including events that recurrently impact genes with important roles in the cell cycle, chromatin regulation and the JAKSTAT pathway. In particular, we show that mutually exclusive structural alterations involving JAK2 and SH2B3 predominantly underlie pcAECyTCL. In line with the genomic data, transcriptome analysis uncovered upregulation of the cell cycle, JAK2 signaling, NF-κB signaling and a high inflammatory response in this cancer. Functional studies confirmed oncogenicity of JAK2 fusions identified in pcAECyTCL and their sensitivity to JAK inhibitor treatment. Our findings strongly suggest that overactive JAK2 signaling is a central driver of pcAECyTCL, and consequently, patients with this neoplasm would likely benefit from therapy with JAK2 inhibitors such as Food and Drug Adminstration-approved ruxolitinib.
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Registered trials
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